You’re lying awake in bed at 4 am. – it’s another sleepless night. Your legs are twitching and pulsating, your mind is racing aimlessly with blurred abstract nonsense and the giant purple bags under your eyes continue to darken and grow larger.
Yes, we’ve all been there.
The last thing you need to hear is that your STRESS and LACK OF SLEEP are actually making the problem WORSE!
But, it’s the truth.
And now that you know this, you can do something about it.
As the powerful influence of inflammation continues to move to the forefront of the media, more and more studies are being done to find out just how widespread its effects are. This includes studies I’ll present to you on this website showing that both stress and insomnia increase inflammation levels.
This post provides scientific evidence that insomnia increases inflammation levels. My next post will focus on how stress increases inflammation levels.
The information you’ll read below are short excerpts from the studies. To view the full studies please visit:
“Sleep Loss and Inflammation.”
Janet M. Mullington et al. Best Pract Res Clin Endocrinol Metab. Oct 2010; 24(5): 775–784.
Controlled, experimental studies on the effects of acute sleep loss in humans have shown that mediators of inflammation are altered by sleep loss.
“Sleep duration and biomarkers of inflammation.”
Patel SR et al. Sleep. 2009 Feb;32(2):200-4.
Extremes of sleep duration have been associated with adverse health outcomes. The mechanism is unclear but may be related to increased inflammation. We sought to assess the association between sleep duration and inflammatory biomarkers.
Increases in habitual sleep durations are associated with elevations in CRP and IL-6 while reduced PSG sleep duration is associated with elevated TNFa levels. Activation of pro-inflammatory pathways may represent a mechanism by which extreme sleep habits affect health.
“Sleep Loss Activates Cellular Inflammatory Signaling”
Michael R. Irwin et al. Biol Psychiatry. 2008 Sep 15;64(6):538-40.
Accumulating evidence suggests that sleep disturbance is associated with inflammation and related disorders including cardiovascular disease, arthritis, and diabetes mellitus. This study was undertaken to test the effects of sleep loss on activation of nuclear factor (NF)-kappaB, a transcription factor that serves a critical role in the inflammatory signaling cascade.
“Chronic Insomnia and Stress System.”
Maria Basta, M.D. et al. Sleep Med Clin. Jun 2007; 2(2): 279–291.
In insomnia, which is a very common sleep disorder, objective sleep measures, EEG activity, physiologic findings, HPA axis activity and inflammation markers suggest that it is not a state of sleep loss, but a disorder of hyperarousal present both during the night and the daytime.
The finding that pro-inflammatory cytokines’ IL-6 and TNFa daytime secretion is elevated in insomniacs, considering their role in subjective complaints of fatigue and poor performance, may lead to novel approaches to treat insomnia.
“The effects of 40 hours of total sleep deprivation on inflammatory markers in healthy young adults.”
Frey DJ et al. Brain Behav Immun. 2007 Nov;21(8):1050-7.
Inflammatory cytokines are released in response to stress, tissue damage, and infection. Acutely, this response is adaptive; however, chronic elevation of inflammatory proteins can contribute to health problems including cardiovascular, endocrine, mood, and sleep disorders.
Our findings suggest that one night of sleep loss triggers a stress response that includes stimulation of both pro- and anti-inflammatory proteins in the healthy young subjects tested under our experimental conditions.
“Effect of sleep loss on C-reactive protein, an inflammatory marker of cardiovascular risk.”
Meier-Ewert HK et al. J Am Coll Cardiol. 2004 Feb 18;43(4):678-83.
Both acute total and short-term partial sleep deprivation resulted in elevated high-sensitivity CRP concentrations, a stable marker of inflammation that has been shown to be predictive of cardiovascular morbidity. We propose that sleep loss may be one of the ways that inflammatory processes are activated and contribute to the association of sleep complaints, short sleep duration, and cardiovascular morbidity observed in epidemiologic surveys.
“Sleep Restriction Increases the Risk of Developing Cardiovascular Diseases by Augmenting Proinflammatory Responses through IL-17 and CRP.”
Wessel M. A. et al. PLoS One. 2009;4(2):e4589. doi: 10.1371/journal.pone.0004589. Epub 2009 Feb 25.
Sleep restriction, leading to deprivation of sleep, is common in modern 24-h societies and is associated with the development of health problems including cardiovascular diseases. Our objective was to investigate the immunological effects of prolonged sleep restriction and subsequent recovery sleep, by simulating a working week and following recovery weekend in a laboratory environment.
5 nights of sleep restriction increased lymphocyte activation and the production of proinflammatory cytokines including IL-1beta IL-6 and IL-17; they remained elevated after 2 nights of recovery sleep, accompanied by increased heart rate and serum CRP, 2 important risk factors for cardiovascular diseases. Therefore, long-term sleep restriction may lead to persistent changes in the immune system and the increased production of IL-17 together with CRP may increase the risk of developing cardiovascular diseases.
For tips on putting an end to your sleepless nights, please visit these pages: